- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
Outpatient burn care
and can leave the skin relatively unharmed between the point of entry and exit. Evaluating electrical injuries and in particular, differentiating between them and injuries from electric arcs (which only cause heat) is extremely difficult, and as a result, should only be carried out in a specialized center. Patients should only receive outpatient treatment in exceptional cases for tiny burns from sparks. Contact with household electricity should always result in shortterm observation of the patient’s heart and circulatory functions in order to detect any resulting complications. The electricity’s entry and exit points are usually deep lesions with a poor prognosis for healing. In this case, inpatient treatment is usually also indicated.
Self-inflicted or externally-inflicted injuries
If the burn or scald is the result of a self-inflicted injury or one inflicted by a third party, the person must receive inpatient treatment regardless of the extent of the local damage. Even when dealing with small injuries, this is an important step as it serves to remove the patient from the dangerous place and determine the exact cause of the trauma. In these cases it can sometimes be necessary to get family members, caretakers, and even the police involved. Offering the injured person outpatient treatment is not indicated, because in these types of cases further injuries to the patient are to be expected [23].
Chemical burns
The effect of corrosive chemicals to our skin causes coagulative necrosis if the chemical is an acid. Depending on the length of exposure, these chemicals can cause different degrees of damage similar to burns [22]. On the other hand, bases more often cause liquefactive necrosis, which causes the tissue to liquefy. Similar to acid, this can also result in varying degrees of damage. Chemical burns caused by hydrofluoric acid represent a special case, since after penetrating the skin, the acid often causes necrosis which stretches deep into the tissue and even destroys bone.
The first main step when treating such injuries is to rinse them with copious amounts of water. This dilutes the damaging substance while at the same time washing it out. Antidotes are also used in special cases, for example when treating chemical burns caused by hydrofluoric acid. In this case, the affected area is coated with calcium gluconate and if the extremities are injured, calcium gluconate is also administered intra-arterially [22]. When providing initial treatment it is often difficult to evaluate the effects of a chemical burn as well as its progression, which means that in this case the injured person must be monitored at close intervals after receiving inpatient treatment, even if injuries appear to be minor. People with chemical burns caused by hydrofluoric acid must always be transferred to a specialist clinic to receive inpatient treatment.
Treatment
Initial treatment
There is no question that immediately cooling the tissue to under 44 degrees Celsius after a trauma is sensible, since allowing the tissue to remain at a high temperature would lead to even more extensive tissue necrosis. The method used to cool the tissue as well as the length of time the tissue should be cooled are the subjects of much debate, however.
It is generally recommended to use cool tap water for a period of up to 30 minutes. However, when doing so one must take care of not to cool too large of an area due to the risk of hypothermia. Cooling the area not only reduces tissue temperature to more normal levels but further stabilizes mast cells. As a result, the release of inflammatory mediators is decreased, pain is alleviated, and edema is reduced [24]. Using extremely cold water and/or ice packs or ice should be avoided, since the resulting reduction in capillary circulation can actually increase the amount of tissue damage.
Based on the aforementioned, cooling a burn wound is more of an immediate emergency procedure to be carried out at the location of the accident, and as a result, represents a method of first aid which one can carry out themselves or can be provided by a layperson. On the other hand, in the scope of initial medical treatment by a physician, cooling the burn wound is only recommended when tissue is severely overheated [25].
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Pain therapy
Burns are extremely painful, especially superficial burns affecting the dermis. This strong burning pain can continue for several hours and can also reappear due to sticking dressings and/or repeatedly manipulating the burn wound while providing treatment or changing bandages. Deep burn wounds are often less sensitive and are associated with reduced pain due to the destruction of the skin’s nerve receptors. Providing sufficient pain therapy represents an important first step in treating all burns [26].
Providing non-steroidal anti-inflammatory drugs (NSAID) at an early stage should be considered. Drugs containing acetylsalicylic acid should not be used due to coagulopathy resulting from platelet function disorders.
When treating kids, the use of an age-appropri- ate and weight-appropriate dose of acetaminophen is recommended. If this first stage of pain therapy is not sufficient, a combination using codeine or metamizole or an orally-administered opiate should be considered. Significantly agitated patients benefit from the use of a fast-acting benzodiazepine, which will have a sedative effect. For the first few days a sufficient number of analgesics should prescribed as the standard medication. Prescribing an increased dose for bandage changing procedures, physical therapy, and/or for nights may be necessary. When it comes to the use of analgesics, one must always consider the patient’s additional alcohol intake or, if applicable, factor other addictive disorders into a calculated pain therapy program.
If a patient has significant and/or uncontrollable pain, they should not receive outpatient treatment but rather be transferred to an inpatient setting. Once there, pain medication should be administered intravenously. The use of local anesthetics, or rather injecting local anesthetics into the area of the burn wound should not be carried out within the course of burn treatment.
Local treatment
Burn blisters
Particularly in the case of dermal burns, part of the epidermis rises up in the form of a thin blister. In deeper burns, the necrotic area is thicker, which
means that these blisters usually do not form. The substance inside the blister shows the disruptive effect on wound healing [27]. Nevertheless, an intact blister represents a closed wound, which reduces the risk of infection. As a result, the proper method of handling blisters is a subject of much debate. In our own procedures, with the exception of extremely tiny blisters and thick blisters located on the palms of the hands or the soles of the feet, we completely remove all blisters. It is imperative that all blisters in the area to be treated are completely removed, particularly when planning to use modern wound dressings. Since torn blisters do not offer any protection against infection, the wound needs to be treated with topical substances anyway. Similarly, in order to prevent the hair from sticking to the wet wound, any body hair remaining in the wound area must also be removed, with the exception of the eyebrows.
Debridement
As previously mentioned, all burn wounds must be debrided. Removal of the blisters is carried out either using scissors and tweezers, with a moist compress, or a soft brush. Manipulating the wound in this way requires the patient’s pain to be sufficiently numbed, and as a result, such procedures are often carried out while the patient is anesthetized. The goal of this procedure should always be to thoroughly clean the wound bed. This is the only way to properly evaluate the depth of the burn as well as initiate proper wound treatment procedures. Mild liquid soap, or better yet, Lavasept or octenide solution are perfectly suitable for cleaning contaminated wounds. In our procedures, we completely refrain from using products which contain iodine to avoid contaminating our waste water [28]. Extremely adhesive substances such as tar, asphalt, or lubricants can be removed using baby oil or butter.
Surface treatment/Topical substances
The rationale for using topical substances in the treatment of burns is primarily to reduce superinfection of the burn wound. In addition, particularly when it comes to the superficial wounds which are usually the focus of outpatient treatment, these sub-
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Outpatient burn care
stances should not slow down reepithelialization. Furthermore, priority is given to the patient’s comfort with an almost painless or truly painless application [29].
A number of substances more or less fulfill these criteria and as a result, are suitable for use when treating superficial burn wounds.
Povidone-Iodine
Povidone-Iodine (PVP-I) is effective against most germs which are relevant to the treatment of burn wounds. However, it is important to take note of the substance’s considerable cytotoxicity, which can slow down the wound healing process [30]. Furthermore, its absorption toxicity must also be considered. A contraindication exists in case of hyperthyroidism, dermatitis herpetiformis, hypersensitivity to iodine, as well as use before and after radioiodine therapy (Kramer). In our procedures, ointments containing iodine are only used for deep burn wounds under consideration of the contraindications, since the iodine also has an drying effect on the skin which makes it easier to operate on later. Liposome capsules filled with PVP-I in hydrogel form are an affordable galenical which have a reduced iodine content and are more gentle on the wound. As a result, this iodine preparation (Repithel, Mundipharma GmbH, Limburg, Germany) is also suitable for follow-up treatment of transplanted wounds.
Silver sulfadiazine (Flamazine ) and other silver products
Dressings containing silver have been used to cover wounds since ancient times. The free silver ions can damage bacteria cell walls, and silver sulfadiazine bonds with bacterial DNA. This means Flamazine has a bacteriostatic and bactericidal effect, and is suitable for all burn wounds [31]. However, when using Flamazine, as is the case with all silver ion applications, one must always take its cytotoxic effect (with slowed wound healing) into consideration. In addition, Flamazine forms a residue on the wound (“Flamazine eschar”) which makes evaluating the wound after several days significantly more difficult. Due to these drawbacks, we completely refrain from using Flamazine in our own procedures. New products are currently offered like Acticoat and
Mepilex Ag . There benefit is that do not require daily dressing changes like Flammazine, but the use of silver products are more and more under discussion.
Polyhexanide (PHMB)
In the past few years, a new topical antiseptic has gained popularity in burn wound treatment thanks to it also having a wide range of effects and extremely low cytotoxicity when it comes to keratinocytes and fibroblasts. Polyhexanide was primarily sold as a raw material under the name Lavasept by the company Fresenius, and customers had to prepare ready-to- use gels and solutions themselves. But since then a number of manufacturers have created such ready- to-use solutions or gel forms of polyhexanide which, as a result, are now available for use in burn wound treatment. The advantage of the limpid gel or limpid solution is that it doesn’t change the color of the wound, which means the wound can be evaluated at any time while providing treatment. Because it is highly diluted, Lavasept gels can be used in the wound area not only in short-term but also longterm applications. The applied solutions or gels do not cause any pain, which means children can tolerate them as well. Polyhexanide is the first known wound antiseptic with a selective mechanism of action. This is due to a strong effect on the acidic phospholipid bacterial cell membranes but only a slight effect on neutral phospholipid human cell membranes. This explains polyhexanide’s extremely minimal cytotoxicity. Due to its molecule size, based on the current state of knowledge we can assume that polyhexanide is not absorbed by the body and as a result, only has an effect on the area of application [32].
In day-to-day clinical practice, gel preparations which use polyhexanide have proved to be of great value in the moist treatment of superficial burn wounds. We use the solutions both as a gentle method of disinfecting wounds when providing initial treatment and as part of subsequent dressing changes.
Obsolete and unnecessary substances
Dyes and organic mercury compounds should be viewed as obsolete and unnecessary for use as burn wound antiseptics. In addition, hydrogen peroxide is
437